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丙烯腈暴露大鼠红细胞中的血红蛋白降解、脂质过氧化及钠钾ATP酶抑制作用

Hemoglobin degradation, lipid peroxidation, and inhibition of Na+/K(+)-ATPase in rat erythrocytes exposed to acrylonitrile.

作者信息

Farooqui M Y, Mumtaz M M, Ghanayem B I, Ahmed A E

机构信息

Department of Pathology, University of Texas Medical Branch, Galveston 77550.

出版信息

J Biochem Toxicol. 1990 Winter;5(4):221-7. doi: 10.1002/jbt.2570050404.

DOI:10.1002/jbt.2570050404
PMID:1965727
Abstract

The effect of acrylonitrile (VCN) on erythrocyte lipid metabolism was investigated in vitro in metabolically active red cells from male Sprague-Dawley rats containing three types of hemoglobins: oxyhemoglobin, methemoglobin, and carbon monoxyhemoglobin. VCN at the concentration of 10 mM rapidly depleted erythrocyte glutathione (GSH) (75% of control) and induced lipid peroxidation (274% of control). Degradation of oxy- and methemoglobin was directly proportional to the extent of lipid peroxidation (r = 0.89). Addition of glucose to the incubation medium decreased hemoglobin degradation while it slightly increased VCN-induced lipid peroxidation. The highest amount of lipid peroxidation occurred in erythrocytes containing carbon monoxyhemoglobin and glucose. In the isolated red cell membranes incubated with 10 mM VCN, the lipid peroxidation was 400% of controls. VCN (25 mM) noncompetitively inhibited erythrocyte membrane Na+/K(+)-ATPase activity and the degree of inhibition was inversely proportional to the reaction temperature (r = -0.88). These findings indicate that the VCN induced hemoglobin degradation and lipid peroxidation are two extremes of a spectrum of oxidative damage in red cells leading to a change in physical state of membrane structure causing inhibition of adenosine triphosphate (ATPase) activity.

摘要

在体外对雄性斯普拉格 - 道利大鼠含有三种血红蛋白(氧合血红蛋白、高铁血红蛋白和碳氧血红蛋白)的代谢活跃红细胞进行了丙烯腈(VCN)对红细胞脂质代谢影响的研究。浓度为10 mM的VCN迅速消耗红细胞谷胱甘肽(GSH)(降至对照组的75%)并诱导脂质过氧化(增至对照组的274%)。氧合血红蛋白和高铁血红蛋白的降解与脂质过氧化程度直接相关(r = 0.89)。向孵育培养基中添加葡萄糖可减少血红蛋白降解,同时略微增加VCN诱导的脂质过氧化。脂质过氧化量最高发生在含有碳氧血红蛋白和葡萄糖的红细胞中。在与10 mM VCN孵育的分离红细胞膜中,脂质过氧化是对照组的400%。VCN(25 mM)非竞争性抑制红细胞膜Na+/K(+)-ATP酶活性,抑制程度与反应温度成反比(r = -0.88)。这些发现表明,VCN诱导的血红蛋白降解和脂质过氧化是红细胞氧化损伤谱的两个极端,导致膜结构物理状态改变,从而抑制三磷酸腺苷(ATP酶)活性。

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